All aspects of Chlamydia survival are intimately linked to the cell biology of its host. Recent advances in cell biological techniques and new tools to perform loss‐of‐function experiments in mammalian cells have accelerated one's understanding of the extent to which Chlamydia manipulates the host. Homotypic fusion of C. trachomatis inclusions could serve to consolidate resources and reduce competition among multiple growing inclusions. It is clear that Incs on early inclusions likely play important roles in remodeling the nascent inclusion to segregate from the endolysosomal pathway and maintain single inclusion morphology in fusogenic Chlamydia species. However, the role played by soluble effectors secreted early or even during entry should not be discounted when considering early interactions with host cell biology. Of host sphingolipids (SLs), only sphingomyelin, and not glucosylceramide, is delivered to the chlamydial inclusion , suggesting highly specific interactions with host pathways. Multivesicular bodies (MVBs) are late endocytic compartments in which the limiting membrane of endosomes has invaginated into the lumen to form intraluminal vesicles containing membrane proteins destined for degradation. Much of the focus of investigations into chlamydial anti‐immune strategies has centered on the interruption of innate immune signaling pathways. Given the long evolutionary history of the association of Chlamydia spp. with eukaryotic cells, these bacteria are expected to reveal new insights into basic aspects of eukaryotic cell biology, primordial mechanisms of cell autonomous innate immunity, and novel pathogenic strategies.